Prostacyclin (PGI2) and Platelet Adherence to Vascular Cells: Platelet adherence and PGI2 release were studied using cultures of endothelial cells (EN) and fibroblasts (F) from vessels of human umbilical cords, and mouse hemangioendothelioma (MHE) cells. MHE cells form vascular channels in vivo which develop thrombi as part of a consumption coagulopathy. A radioimmunoassay for 6-keto-PGF1 alpha was used to measure PGI2 released from cell monolayers incubated with 0.5U bovine thrombin or incubation medium control (IM). For platelet adherence studies, 51Cr-labeled platelets were added to untreated or 1 mM aspirin (ASA)-treated monolayers after IM or 0.5U thrombin. In additional adherence studies, exogenous PGI2 was added before thrombin and platelets. Concentrations of 6-keto-PGF1 alpha (nM) after thrombin were: 62.5 plus or minus 8.8 venous EN, 9.2 plus or minus 2.4 arterial EN, and 3.0 for F, MHE and ASA-treated venous EN. Incubation with 150 nM exogenous PGI2 decreased thrombin-induced platelet adherence to ASA-treated venous EN (52 to 4 percent), arterial EN (61 to 10 percent), MHE (65 to 3 percent), F (75 to 24 percent) and to empty culture dish controls (81 to 43 percent). The failure of PGI2 to produce more effective inhibition of platelet adherence to non-endothelial surfaces suggests that the endothelium may possess additional non-thrombogenic components.